It is considered the most contagious infectious disease that impacts human life. Moreover, leprosy still threatens public health worldwide despite the reduction of infection incidences due to antimicrobial treatments. However, healing from the disease require early timely detection and drug administration (Franco-Paredes & Rodriguez-Morales, 2016). Otherwise, the patients affected would be paralyzed. Hence, it is necessary to study the disease and conduct surveillance to curb its spread.
Leprosy and Impact on Patients
Leprosy is a disease that manifests upon infection by Mycobacterium leprae, which is an intracellular pathogen surviving exclusively in an anaerobic environment. Clinical progression of leprosy occurs in two forms: lepromatous and tuberculoid (Farag et al., 2020). The development of lepromatous form of the disease occurs when helper T lymphocytes secrets cytokines which yields proinflammatory reactions against body cells and tissues. Eventually, clinical symptoms of leprosy develop, leading to body deformation (Farag et al., 2020). Sequelae also stem from muscles and nerves destruction resulting to disabilities and social stigmatization of patients.
History of Leprosy Disease
Leprosy (also known as Hansen disease) was considered a curse among religious communities in the 18th century. It is believed that the first incidence occurred in India, then it spread advanced to the Middle East. The spread of leprosy in Europe occurred in 300BC when soldiers of Alexander the Great were migrating between continents. Eventually, the disease became a worldwide pandemic in the post-antibiotic era, with over 213 899 cases by 2014 (Franco-Paredes & Rodriguez-Morales, 2016). Currently, genetic profiling has unveiled that not only Mycobacterium leprae stands as the etiological agent of leprosy by also Mycobacterium lepromatosis.
Epidemiology of Leprosy Disease
The Hansen disease is endemic in tropical regions with a high prevalence rate in low and middle-income countries. However, since 1980 when antibiotics against the disease were introduced, its incidence has drastically reduced. Some nations like Brazil and India have still not reached the expected case numbers of leprosy, making it a challenge to public health (Franco-Paredes & Rodriguez-Morales, 2016). Early detection through surveillance and immediate enrollment of clients into antibacterial therapy stands as the control measures which have effectively worked against leprosy.
Physiology of Mycobacterium leprae
The genome of Mycobacterium leprae contains 2770 genes that encode for the structural and functional proteins. It is a circular deoxyribonucleic acid (DNA) with approximately 3.3 million base pairs. Moreover, the guanine-cytosine content of the DNA is 57.8 percent. The genetic material and cytoplasmic contents are enclosed by a semipermeable plasma membrane (Franco-Paredes & Rodriguez-Morales, 2016). The membrane is constituted by a lipid bilayer and surface proteins, which acts as the antigens for serological diagnosis. Enclosing the lipid membrane is the capsule containing polysaccharides and arabinogalactans, which bind mycolic acids and lipoarabinomannan (Franco-Paredes & Rodriguez-Morales, 2016). Mycobacterium leprae is an Actinomycete bacterium belonging to the taxonomic class called Schizomycetes and Mycobacteriaceae family. It is a slightly curved bacilliform bacterium with dome-shaped ends (Franco-Paredes & Rodriguez-Morales, 2016). The bacterium grows intracellular in Schwann cells and macrophages.
Pathological Manifestations of Leprosy
Transmission of Mycobacterium leprae happens when an infected individual gets into close contact with a healthy person. The most common mode of transmission is through the exchange of nasopharyngeal secretions. The microorganism gets into host cells through the phagocytic action of antigen-presenting cells then escapes lysis through inhibition of enzymatic actions within the phagolysosome (Mohanty et al., 2020). The cellular immune reactions involving the production of cytokines in response to the pathogen initiates proliferation of type-1 and type-2 helper T cells (Franco-Paredes & Rodriguez-Morales, 2016). Consequently, the tuberculoid and lepromatous lesions develop in the infected tissues, such as the skin. The presentation of neuropathic effects leads to loss of sensitivity of the peripheral verves. Pulmonary tuberculosis often develops because of lung tissue damage (Farag et al., 2020). Cardiac failure and renal dysfunctions are always recorded due to type 2 helper T cells reactions.
Symptoms of Leprosy
Clinical presentation of leprosy relies heavily on host immune reactions and can follow prolonged incubation of averagely 2 to 4 years. Typical leprosy is defined by sensitive lesions on the skin, which are painful and fluctuating fever characterized by chills. As the disease advances to severe stage, hypochromic spots and erythematous plagues develops. Uncommon symptoms include loss of limbs and sight at the advanced stages of the disease (Franco-Paredes & Rodriguez-Morales, 2016). The administration of multidrug therapy suppresses the development of lesions by killing the pathogen and suppressing cytokine-mediated tissue destructions.
Prevention and Cure for Leprosy
Conventional medication has, for long, been effective in leprosy treatment. Antibiotics like rifampicin, ofloxacin, and sulfones are used to inhibit bacterial growth by tampering with membrane integrity and DNA synthesis (Franco-Paredes & Rodriguez-Morales, 2016). Moreover, multidrug therapy is currently used to remedy leprosy. The drugs are augmented to overcome resistance, kill the pathogen, and regulate immune reactions. Holistically, antibiotic therapy is combined with social inclusion to alleviate stigma in patients (Mohanty et al., 2020). Prevention through early diagnosis and prompt administration of drugs is effective in reducing transmission and severe clinical complications.
Conclusion
In conclusion, leprosy is still a threat to public health globally. It a contagious disease with debilitating impacts on the body at the cellular level. It attacks the immune system and uses the body’s defense to manifest its clinical complications. Antimicrobial therapy and surveillance have been effective in leprosy management. However, further research on avenues to overcome mutations and antimicrobial resistance in which bacterial development with time should be enforced to imitate preparedness to curb pandemic can occur anytime.
References
Farag, A. G., Askary, S. A., Fathy, W. M., Elbassal, F., Azzam, A. A., Tayel, N. R., Karim, S. S. A., Shehata, W. A. (2020). Relationship between sCD163 and mCD163 and their implication in the detection and typing of leprosy. Clinical, Cosmetic and Investigational Dermatology, 13, 379–389. Web.
Franco-Paredes, C., & Rodriguez-Morales, A. J. (2016). Unsolved matters in leprosy: a descriptive review and call for further research. Annals of clinical microbiology and antimicrobials, 15(1), 1-10.
Mohanty, P. S., Naaz, F., Bansal, A. K., Kumar, D., Singh, H., Katara, P., Soni, N., Patil, S. A., Sharma, S., Arora, M., Singh, M. (2020). Molecular detection of Mycobacterium leprae using RLEP-PCR in post elimination era of leprosy. Molecular Biology Research Communications, 9(1), 17-22. Web.